The paper describes the CeA-LPB pathway as an inhibitory amygdalo-parabrachial circuit that regulates pain-related activity in parabrachial neurons. Its efficacy is reported to be suppressed in chronic pain.
First-pass extracted concept
CeA-LPB pathway
Candidate: concept label1 source documents4 linked claims
Live refresh every 5sNext refresh in 5s
Aliases
amygdalo-parabrachial pathway
Extracted Explainers
What the tool is doing
What problem it solves
What it does not solve
Evidence Snippets
Supporting Sources
Linked Claims
Optogenetic stimulation of the CeA-LPB pathway suppresses acute pain, whereas inhibition of this pathway in naive animals evokes pain behaviors.
Quoted textsource-backed
Further, optogenetically stimulating this pathway suppresses acute pain, and inhibiting it, in naive animals, evokes pain behaviors.
In rats and mice, LPB contains few GABAergic neurons and most of its GABAergic inputs arise from CeA neurons expressing dynorphin, somatostatin, and/or corticotropin releasing hormone.
Quoted textsource-backed
We show that, in both rats and mice, LPB contains few GABAergic neurons, and that most of its GABAergic inputs arise from CeA. These CeA GABA neurons express dynorphin, somatostatin, and/or corticotropin releasing hormone.
Chronic pain is associated with amplified activity of parabrachial neurons in mice and this amplification is related to suppressed inhibition from CeA to LPB neurons.
Quoted textsource-backed
Here we demonstrate that similar activity amplification occurs in mice, and that this is related to suppressed inhibition to lateral parabrachial (LPB) neurons from the CeA in animals of either sex.
The CeA-LPB pathway is critically involved in pain regulation and in the pathogenesis of chronic pain.
Quoted textsource-backed
These findings demonstrate that the CeA-LPB pathway is critically involved in pain regulation, and in the pathogenesis of chronic pain.